Posts Tagged ‘lv dysfcuntion’

LV dysfunction , perhaps  is  the most common  medical term used by  physicians  world over.But surprisingly , It is not easy to infer what they mean by it ! The term literally means left ventricle is not functioning all right .

LV dysfunction can be classified by many  ways.

  • Symptomatic vs Asymptomatic
  • Global vs  Regional
  • Reversible vs Permanent
  • Systolic vs  Diastolic
  • Ischemic vs Nonischemic
  • Primary vs  Secondary ( Muscle vs valve  etc)

If you analyse the above classification LV dysfunction can mean different things to different people , at different times.Though systolic dysfunction ,  as reflected by low EF % ( Less than 50% ) is the major cause of LV dysfunction  the issue is not simple.

Is coronary artery disease ( CAD  ) a must for LV to  become dysfunctional ?

No , not at all .CAD  is the leading cause of LV dysfunction .Primary muscle disorders -cardiomyopathy is an equally common entity. Valve disorders especially  aortic valve stenosis is   another common cause for LV dysfunction. Further ,  systemic hypertension, diabetes mellites, renal failure, can result in serious impairment of LV function .Some drugs ( Adriamycin ) can either precipitate or aggravate LV dysfunction.

If  physicians themselves are confronted with such complexity , how are ,  our other medical  colleagues  (Forget about the patients !   ) will understand  the concept of LV dysfunction.

But , the  crux of the matter is every doctor believes  LV dysfunction is synonymous with low ejection fraction. A surgeon or an anesthetist is quiet happy to operate  if the ejection fraction is above 60% .

Can a patient  have significant LV dysfunction with normal Ejection fraction ? (EF )

Yes , this can occur in advanced degrees of diastolic dysfunction, where cardiac contractility is normal but

fails to relax adequately .

Is diastolic dysfunction less dangerous than systolic dysfunction?

May be , that is the dominant opinion   , but  there are sufficient evidence  emerging  that opinion is wrong.The main reason for diastolic dysfunction  to send a ” not so sinister signal ” is over diagnosis of  grade 1 diastolic dysfunction in the general population  . The echocardiologists considered it fashionable for a quiet a longtime (Many have changed since then !)  to report all patients  with reversed E :A ratio in the mitral inflow doppler profile as diastolic dysfunction. This has resulted in  thousands  of  asymptomatic , healthy people getting  labelled  as grade 1 diastolic dysfunction  undermining the importance of this entity.

The fact of the matter is true diastolic dysfunction is indeed dangerous , if not more dangerous than systolic dysfunction  for the simple reason ,  there is  no specific treatment for this condition

To improve the specificity to diagnose genuine LV diastolic dysfunction it is suggested to remove grade 1 diastolic dysfunction from the literature .

Other causes of LV dysfunction with normal EF

  • Some times , there can be wall motion defects  and   mitral regurgitation but still the EF can be normal .
  • Mitral valve dysfunction can be a part of LV dysfunction .The EF is either  not affected as ischemic damage  might be confined to papillary muscle.
  • Vigorous compensation from non ischemic areas  can normalise an EF

What is the difference between LV dysfunction and  LV failure ?

Many times  both these terms are perceived  to convey the same meaning .But it  can  never be used synonymously .Cardiac failure is a clinical entity while LV dysfunction  is  a  derived  technical parameter  by and large an echocardiographic enity. Cardiac failure   is defined classically as a clinical syndrome .(elevated jvp, edema * S 3 rales etc)  Neuroueohormonal activation  can occur with both.

A patient with   LV dysfunction    when destabilsed  develops   LV  failure and after stabilisation of   LV failure he is brought  back to  the baseline  LV dysfunction

*What is the link between LV dysfunction and RV dysfunction ?

RV can not be silent companion when the LV fails  . There always have been link between the two.

LV dysfucntion begets RV dysfunction   and LV failure can trigger a total heart failure

Apart from the classical concept of ventricular interdependence  ,  where  inter ventricular  septum plays a pivotal role , now there is strong evidence  to  prove  both LV and RV myocardial muscle  bundles are interwoven . In fact failing LV drags the muscle bundles over RV also (Friendly pull , let us die together !)  and this is classically seen in idiopathic dilated cardiomyopathy where all four chambers of the heart dilate. There is also biochemical  evidence the RV myocytes deplete thier norepinephrine stores  in LV failure.

Is there an entity called transient  or temporary LV dysfunction ?

The classical chronic reversible LV dysfunction also called hibernating myocardium is a different topic shall be discussed later.

Can acute ischemia cause LV dysfunction  ?

Yes .This can occur during ischemic stunning of myocardium during NSTEMI .This can result in acute pulmonary edema* at times.This can be termed as ischemic LV dysfunction  as there is no myocardial necrosis .

* The pulmoanry edema mentioned here is the  flash pulmonary edema carries very dis prognosis.

What is the cause of LV dysfunction in critical aortic stenosis ?

Is it fibrotic ?

Is it necrotic ?

Is it ischemic ? (Associated CAD )

Or is  it simply  a mechanical inability* to contract  as the outflow is closed ?

There is no specific answer . All the above factors may contribute .*But the fact that  most patients recover full normal LV function  following aortic valve replacement would make the last explanation more likely.

What does the term LV  dysfunction mean to a  cardiac surgeon when he plans  for  a CABG ?

LV dysfunction becomes an important determinant of overall  outcome   in  patients who  are  going  to receive a CABG .The surgeon will have contingent strategies  during peroperative and post operative phase while operating  in hearts with severe LV dysfunction.

How much  of LV function  is going to recover after CABG  ?

This  can not be predicted accurately but CABG  may not  resucitate all dying myocytes and bring life in them .The buttressing effect of blood within the dysfunctional segement can improve contractility and  reduce the wall motion defect(This is an indirect mechanism of improving EF )

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